替比夫定，相关性肌病的临床病理特征。

StephenW

PLoS One. 2016 Sep 9;11(9):e0162760. doi: 10.1371/journal.pone.0162760.
Clinicopathological Features of Telbivudine-Associated Myopathy.Ambang T1,2, Tan JS1,2, Ong S3, Wong KT2, Goh KJ1.
Author information

• 1Division of Neurology, Department of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
• 2Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
• 3Department of Medicine, Queen Elizabeth Hospital, Kota Kinabalu, Sabah, Malaysia.
  

AbstractTelbivudine, a thymidine nucleoside analog, is a common therapeutic option for chronic hepatitis B infection. While raised serum creatine kinase is common, myopathy associated with telbivudine is rare. Reports on its myopathological features are few and immunohistochemical analyses of inflammatory cell infiltrates have not been previously described. We describe the clinical, myopathological and immunohistochemical features of four patients who developed myopathy after telbivudine therapy for chronic hepatitis B infection. All four patients presented with progressive proximal muscle weakness, elevation of serum creatine kinase and myopathic changes on electromyography. Muscle biopsies showed myofiber degeneration/necrosis, regeneration, and fibers with cytoplasmic bodies and cytochrome c oxidase deficiency. There was minimal inflammation associated with strong sarcolemmal overexpression of class I major histocompatibility complex (MHC class I). Upon withdrawal of telbivudine, muscle weakness improved in all patients and eventually completely resolved in three. In our series, telbivudine-associated myopathy is characterized by necrotizing myopathy which improved on drug withdrawal. Although the occasional loss of cytochrome c oxidase is consistent with mitochondrial toxicity, the overexpression of MHC class I in all patients could suggest an underlying immune-mediated mechanism which may warrant further investigation.


PMID:27611456DOI:10.1371/journal.pone.0162760

StephenW

公共科学图书馆之一。 2016年9月9日; 11（9）：e0162760。 DOI：10.1371 / journal.pone.0162760。
替比夫定，相关性肌病的临床病理特征。
安邦火山T1,2，谭JS1,2，翁S3，黄KT2，吴作栋KJ1。
作者信息

    神经内科，医学系，医学系，马来亚大学，吉隆坡，马来西亚1区。
    病理学，医学系，马来亚大学，吉隆坡，马来西亚教研室。
    医药，伊利沙伯医院，哥打京那巴鲁，沙巴，马来西亚3Department。

抽象

替比夫定，胸苷核苷类似物，是慢性乙型肝炎感染的共同治疗选择。虽然提出了血清肌酸激酶是共同的，替比夫定相关肌病是罕见的。其myopathological特征的报告是炎性细胞浸润数和免疫组织化学分析尚未如前所述。我们描述的替比夫定谁治疗慢性乙型肝炎病毒感染后出现肌病例患者临床，myopathological和免疫组化特征。表现为进行性近端肌无力，血清肌酸激酶升高和肌电肌病改变所有4名患者。肌肉活检显示肌纤维变性/坏死，再生，纤维与细胞质体和细胞色素C氧化酶缺乏症。有一个与I类主要组织相容性复合体细胞膜强表达（MHC I类）相关的微量炎症。替比夫定后撤出，肌肉无力，所有患者改善，最终在三个彻底解决。在我们的系列中，替比夫定相关性肌病的特点是坏死性肌病这在停药改善。虽然细胞色素C氧化酶偶尔损失与线粒体毒性一致，MHC I类所有患者的过度表达可能表明这可能需要进一步调查潜在的免疫介导机制。

结论：
    27611456
DOI：
    10.1371 / journal.pone.0162760

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StephenW

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